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柚皮素对西维因诱导的小鼠神经母细胞瘤细胞神经毒性的神经保护作用。

Neuroprotective role of naringenin on carbaryl induced neurotoxicity in mouse neuroblastoma cells.

作者信息

Muthaiah Vijaya Prakash Krishnan, Venkitasamy Lavanya, Michael Felicia Mary, Chandrasekar Kirubhanand, Venkatachalam Sankar

机构信息

Department of Anatomy, Dr. ALM PGIBMS, University of Madras, Taramani Campus, Chennai, India.

出版信息

J Pharmacol Pharmacother. 2013 Jul;4(3):192-7. doi: 10.4103/0976-500X.114599.

DOI:10.4103/0976-500X.114599
PMID:23960424
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3746302/
Abstract

OBJECTIVE

Neuroprotective effect of naringenin against carbaryl toxicity was studied in mouse neuroblastoma cell line.

MATERIALS AND METHODS

Mouse neuroblastoma cells (Neuro 2A) obtained from National Center for Cell Sciences, Pune, India were either exposed to carbaryl or pre-treated with naringenin (a flavonoid prepared from grape fruit) before their exposure to carbaryl. Results were analyzed using MTT [3-4,5-Dimethylthiazol-2-yl)-2,5-diphenltetrazolium bromide] assay for cell viability, FACS (fluorescence assisted cell sorting) analysis for apoptotic and necrotic cell populations, DCFH-DA (2,7-dichlorofluorescin-diacetate) assay for Reactive Oxygen Species (ROS) visualization, JC-1 staining for determining mitochondrial membrane potential and real-time PCR for quantifying pro and anti-apoptotic gene expression.

RESULTS

Exposure to naringenin resulted in better survival of Neuro 2A cells which were subsequently subjected to carbaryl toxicity. Treatment with naringenin was found to reduce the oxidative stress by decreasing the ROS and was found to maintain the integrity of mitochondrial membrane potential. It was also found to downregulate pro-apoptotic genes (BAX and Caspase-3) while upregulating anti-apototic gene (Bcl2).

CONCLUSION

The results of this pilot study underline the potential of naringenin in treating carbaryl induced neurotoxicity and further studies are warranted to establish the effect of naringenin in vivo conditions.

摘要

目的

在小鼠神经母细胞瘤细胞系中研究柚皮素对西维因毒性的神经保护作用。

材料与方法

从印度浦那国家细胞科学中心获得的小鼠神经母细胞瘤细胞(Neuro 2A),要么暴露于西维因,要么在暴露于西维因之前用柚皮素(一种从葡萄柚中制备的类黄酮)进行预处理。使用MTT [3-(4,5-二甲基噻唑-2-基)-2,5-二苯基四氮唑溴盐] 法分析细胞活力,通过流式细胞术(FACS)分析凋亡和坏死细胞群体,用2,7-二氯荧光素二乙酸酯(DCFH-DA)法观察活性氧(ROS),用JC-1染色法测定线粒体膜电位,并通过实时定量PCR定量分析促凋亡和抗凋亡基因的表达。

结果

暴露于柚皮素能使随后遭受西维因毒性的Neuro 2A细胞更好地存活。发现用柚皮素处理可通过降低ROS来减轻氧化应激,并能维持线粒体膜电位的完整性。还发现它能下调促凋亡基因(BAX和半胱天冬酶-3),同时上调抗凋亡基因(Bcl2)。

结论

这项初步研究的结果强调了柚皮素在治疗西维因诱导的神经毒性方面的潜力,有必要进一步开展研究以确定柚皮素在体内条件下的作用。

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